Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Protective effect of S-allyl cysteine against cerebral ischemia/reperfusion injury in experimental rats

Xing Liu, Fang Wang, Qian Han , Linshan Zhao

Department of Neurology, Tian Jin 4th Centre Hospital, Tianjin 300000, China;

For correspondence:- Qian Han Email: xingxing.11@163.com Tel:+862226249182

Accepted: 22 August 2021 Published: 30 September 2021

Citation: Liu X, Wang F, Han Q, Zhao L. Protective effect of S-allyl cysteine against cerebral ischemia/reperfusion injury in experimental rats. Trop J Pharm Res 2021; 20(9):1895-1902 doi: 10.4314/tjpr.v20i9.16

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the protective effect of S-allyl cysteine (SAC) against cerebral ischemia reperfusion injury (CRI) in rats.

Methods: The protective effect of SAC was determined in a male Wistar rat model of middle cerebral artery occlusion (MCAO)-stimulated transient focal ischemia, followed by reperfusion. Cerebral ischemia reperfusion injury was induced via 90 min of MCAO, followed by 24-h reperfusion. The cerebral infarct size was determined by staining with 2,3,5- triphenyl tetrazolium chloride. The onset of cellular derangement, neurological deficit score and neuronal oedema were determined. In addition, the expressions of CRI markers and inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA).

Results: Rats subjected to CRI showed marked increases in cellular oxidative stress, as evidenced by significant increase in the levels of inflammatory markers, including MDA (p < 0.05), MPO (p < 0.05) and nitric oxide (p < 0.01). In addition, CRI increased the mRNA expression levels of the marker genes TLR4, syndecan-1, CSF, aquaporin-1, OCT3, and RFX1. In contrast, rats pre-treated with SAC prior to CRI displayed reduced levels of inflammatory cytokines, with a near-normal cellular arrangement. SAC treatment significantly reduced the mRNA expression levels of the marker genes in CRI rats.

Conclusion: These findings suggest that SAC may protect the brain of rats from cerebral ischemia-reperfusion injury caused by amplification of oxidative stress and inflammatory signaling. Thus, S-allyl cysteine is a potential therapy for the management of CRI.

Keywords: S-allyl cysteine, Cerebral Ischemia, Reperfusion, Asthma, Inflammation